pH Cancer Research Results

pH, : Click to Expand ⟱

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Type:

Tumor Microenvironment: Cancer cells often thrive in a more acidic environment compared to normal cells. This is partly due to the metabolic processes of cancer cells, which can produce lactic acid and other acidic byproducts. The acidic microenvironment can promote tumor growth and invasion.
Many tumors exhibit an acidic microenvironment. This is largely due to the high rate of glycolysis (often referred to as the Warburg effect), even in the presence of oxygen, leading to lactate production. Acidification is thought to promote invasion, metastasis, and resistance to certain chemotherapies.
The body maintains a relatively stable pH in the blood (around 7.4). However, the pH of tissues can vary, and tumors can exhibit a lower pH.

-Normal tissues have a higher extracellular pH than intracellular pH, in cancer is exactly the opposite. (inversion of the pH gradient).

Cancer cells often overexpress proton pumps (such as V-ATPase) and transporters that actively extrude protons (H⁺) to maintain an intracellular pH conducive to their growth.
Inhibiting these pumps can lead to intracellular acidification and potentially induce apoptosis or render cancer cells more vulnerable to other treatments.

Normal pH levels in the body:
Nasal: ~6.3 pH
Mouth/saliva: 6.2-7.6 pH
Stomach: 1-3 pH
Small Intestine: 5.9-6.8 pH
Colon/Large Intestine: 6.8-7 pH

Scientific Papers found: Click to Expand⟱

1584-

Citrate,

Anticancer effects of high-dose extracellular citrate treatment in pancreatic cancer cells under different glucose concentrations

in-vitro,

PC,

MIA PaCa-2

in-vitro,

PC,

PANC1

tumCV↓, Extracellular sodium citrate significantly reduced cell viability partially due to reduction in intracellular Ca2+ levels
i-Ca+2↓, Intracellular Ca2+ levels were significantly reduced by 28.5 %
TumCMig↓,
CD133↓, decrease in the levels of the stem cell marker prominin I (CD133) following sodium citrate treatment.
pH↑, pH slightly increased upon administration of sodium citrate
eff↑, findings suggest that exogenous sodium citrate treatment, particularly in combination with gemcitabine, may represent a novel therapeutic strategy for treating PDAC.
Ki-67↓, sodium citrate treatment decreased the percentage of Ki67-positive cells
eff↑, sodium citrate treatment may have a more pronounced anticancer effect on glycolytic pancreatic cancer cells with high expression of SLC13A5.

466-

CUR,

Curcumin circumvent lactate-induced chemoresistance in hepatic cancer cells through modulation of hydroxycarboxylic acid receptor-1

in-vitro,

Liver,

HepG2

5 and 10 μM, 24 h

in-vitro,

Liver,

HuT78

GlucoseCon↓,
lactateProd↓,
pH↑,
NO↑,
LAR↓,
Hif1a↓, gene and protein
LDHA↓,
MCT1↓,
MDR1↓,
STAT3↓,
HCAR1↓,

2308-

CUR,

Counteracting Action of Curcumin on High Glucose-Induced Chemoresistance in Hepatic Carcinoma Cells

in-vitro,

Liver,

HepG2

GlucoseCon↓, Curcumin obviated the hyperglycemia-induced modulations like elevated glucose consumption, lactate production, and extracellular acidification, and diminished nitric oxide and reactive oxygen species (ROS) production
lactateProd↓,
ECAR↓,
NO↓,
ROS↑, Curcumin favors the ROS production in HepG2 cells in normal as well as hyperglycemic conditions. ROS production was detected in cancer cells treated with curcumin, or doxorubicin, or their combinations in NG or HG medium for 24 h
HK2↓, HKII, PFK1, GAPDH, PKM2, LDH-A, IDH3A, and FASN. Metabolite transporters and receptors (GLUT-1, MCT-1, MCT-4, and HCAR-1) were also found upregulated in high glucose exposed HepG2 cells. Curcumin inhibited the elevated expression of these enzymes, tr
PFK1↓,
GAPDH↓,
PKM2↓,
LDHA↓,
FASN↓,
GLUT1↓, Curcumin treatment was able to significantly decrease the expression of GLUT1, HKII, and HIF-1α in HepG2 cells either incubated in NG or HG medium.
MCT1↓,
MCT4↓,
HCAR1↓,
SDH↑, Curcumin also uplifted the SDH expression, which was inhibited in high glucose condition
ChemoSen↑, Curcumin Prevents High Glucose-Induced Chemoresistance
ROS↑, Treatment of cells with doxorubicin in presence of curcumin was found to cooperatively augment the ROS level in cells of both NG and HG groups.
BioAv↑, Curcumin Favors Drug Accumulation in Cancer Cells
P53↑, An increased expression of p53 in curcumin-treated cells can be suggestive of susceptibility towards cytotoxic action of anticancer drugs
NF-kB↓, curcumin has therapeutic benefits in hyperglycemia-associated pathological manifestations and through NF-κB inhibition
pH↑, Curcumin treatment was found to resist the lowering of pH of culture supernatant both in NG as well in HG medium.

2249-

MF,

Pulsed electromagnetic fields modulate energy metabolism during wound healing process: an in vitro model study

in-vitro,

Nor,

L929

4mT, 80 Hz

 pulsed burst (burst width, 2 ms; pulse width, 10.5 ms).

*TumCMig↑, PEMFs with specific parameter (4mT, 80 Hz) promoted cell migration and viability.
*tumCV↑,
*Glycolysis↑, PEMFs-exposed L929 cells was highly glycolytic for energy generation
*ROS↓, PEMFs enhanced intracellular acidification and maintained low level of intracellular ROS in L929 cells.
*mitResp↓, shifting from mitochondrial respiration to glycolysis
*other↝, Furthermore, the analysis of ECAR/ OCR basal ratio demonstrated a tendency toward to glycolytic phenotype in L929 cells under PEMF exposure, compared to control group
*OXPHOS↓, PEMFs promoted the transformation of energy metabolism pattern from oxidative phosphorylation to aerobic glycolysis
*pH↑, result of pH detection by flow cytometer indicated the pH level in L929 cells was significantly increased in the PEMFs group compared to the control group
*antiOx↑, PEMFs upregulated the expression of antioxidant or glycolysis related genes
*PFKM↑, Pfkm, Pfkl, Pfkp, Pkm2, Hk2, Glut1, were also significantly up-regulated in the PEMFs group
*PFKL↑,
*PKM2↑,
*HK2↑,
*GLUT1↑,
*GPx1↑, GPX1, GPX4 and Sod 1 expression were significantly higher in the PEMFs group compared to the control group
*GPx4↑,
*SOD1↑,

507-

MF,

Effects of extremely low frequency electromagnetic fields on the tumor cell inhibition and the possible mechanism

in-vitro,

Liver,

HepG2

5 mT and 20 Hz

adherence inhibition rate for Hepg2 and A549 estimated at 18% and 30% respectively

in-vitro,

Lung,

A549

in-vitro,

Nor,

GP-293

MMP↓,
TumCG↓,
ROS↑, key to tumor growth inhibition
*Ca+2↓, Normal 293 T cells showed a significant decrease in the intracellular free calcium ion concentration.
Ca+2↑, The solid tumor cells showed no significant change, while the suspended tumor cells showed a slight increase in the calcium ion concentration
selectivity↑,
i-pH↑, In addition, the intracellular pH of A549 cells increased under the magnetic field.

5611-

NaHCO3,

NaHCO3 enhances the antitumor activities of cytokine-induced killer cells against hepatocellular carcinoma HepG2 cells

vitro+vivo,

HCC,

HepG2

tumCV↓, The results indicated that the viability and growth rate of HepG2 cells were remarkably suppressed when co-cultured with CIK cells or CMCIK at pH 7.4 compared with those of HepG2 cells cultured under the same conditions but at pH 6.5.
TumCG↓,
pH↑, neutralizing the pH (for example, via NaHCO3 administration), could therefore reduce or eliminate this influence.
eff↑, it should be recommended that oncologists routinely prescribe soda water to their patients, particularly during CIK cell therapy.
Imm↑, These results indicated that the acidic environment inhibits the antitumor activity of CIK cells. The activity of CIK cells against HCC is enhanced by NaHCO3 feeding in nude mice

5598-

NaHCO3,

Bicarbonate Increases Tumor pH and Inhibits Spontaneous Metastases

in-vivo,

BC,

MDA-MB-231

mouse

e-pH↑, Here, we show that oral NaHCO3 selectively increased the pH of tumors and reduced the formation of spontaneous metastases in mouse models of metastatic breast cancer. significantly increase the extracellular pH, but not the intracellular pH,
TumMeta↓,
TumCG⇅, Despite a lack of an effect on primary tumor growth, bicarbonate therapy led to significant reductions in the number and size of metastases to lung, intestine, and diaphragm.
Dose↑, The daily intake of bicarbonate was thus calculated to be 36 ± 1.7 mmol/kg/d (9.4 g/m2/d). An equivalent dose in a 70-kg human would be 12.5 g/d (20).

5620-

NaHCO3,

Tumor acidity: From hallmark of cancer to target of treatment

Review,

Var,

e-pH↑, It is very attractive to increase the pHe by a combination of an alkaline diet and bicarbonate therapy (14–16) or by direct local isolated perfusion of the tumor with bicarbonate solutions (17, 18).
TumCG↓, Preclinical and some clinical studies suggest that “direct” tumor deacidification may slow progression or improve therapeutic response (34).
eff↑, Oral administration of sodium bicarbonate can increase the efficacy of doxorubicin and mitoxantrone in model experiments (52, 55).
OS↑, The median overall survival rate in patients whose urine pH became high (>7.0) after the start of therapy was significantly greater than in patients with low urine pH (≤7.0) (16.1 vs 4.7 months; p<0.05) (14).
eff↑, the combination of alkalinization therapy with intravenous vitamin C was also associated with favorable outcomes in patients with small cell lung cancer (SCLC) receiving chemotherapy.
BioAv↑, The use of nanoobjects to deliver buffers due to the enhanced permeability and retention effect (EPR) can overcome such limitations

5617-

NaHCO3,

Microenvironmental alkalization promotes the therapeutic effects of MSLN-CAR-T cells

vitro+vivo,

NA,

Imm↑, alkalization of the microenvironment improves the consistency and high expression of the target antigen MSLN and constitutes a routine method for treating diverse solid cancers via MSLN-CAR-T cells.
eff↑, The combination of microenvironmental alkalinization and CAR-T-cell therapy may represent a standard approach for treating solid cancers.
pH↑, NaHCO3 can regulate the pH value of tumor cells via the sodium bicarbonate cotransporter SLC4A7, which has no significant difference in expression according to tumor type in the Human Protein Atlas database .

5616-

NaHCO3,

DCA,

Bicarbonate and dichloroacetate: Evaluating pH altering therapies in a mouse model for metastatic breast cancer

vitro+vivo,

BC,

MDA-MB-231

umor bearing mice received bicarbonate, DCA, or DCA-bicarbonate (DB) therapies chronically.

OS↑, Survival was longest in mice administered bicarbonate-based therapies.
e-pH↑, This study reported that systemic bicarbonate buffered the extracellular pH in tumors to neutral levels (a pH of 7.2) and inhibited the spread of metastases which led to improved survival.
TumMeta↓,
eff↝, Urine pH in DCA treated mice was the same as measured in untreated mice.
TumCG↝, In our study, treating MDA-MB-231 tumor bearing mice with DCA and DB did not impact primary tumor growth.

5615-

NaHCO3,

immuno,

pH-Responsive Nanoparticles for Cancer Immunotherapy: A Brief Review

Review,

Var,

eff↑, Integrating pH-responsive nanoparticles into immunotherapy is a powerful approach to tackle these challenges because they are able to target the tumor tissues and organelles of antigen-presenting cells (APCs) which have a characteristic acidic microe
eff↑, The incorporation of bicarbonate salts into PLGA nanoparticles enables 33-fold higher loading of the hydrophobic agonist and the rapid rapture of nanoparticles at acidic pH
pH↑,

5614-

NaHCO3,

Targeting the Acidic Tumor Microenvironment: Unexpected Pro-Neoplastic Effects of Oral NaHCO3 Therapy in Murine Breast Tissue

in-vivo,

BC,

NaHCO3-containing drinking water to female C57BL/6j mice. bc

e-pH↑, Oral NaHCO3 therapy increases breast tumor pH in vivo from 6.68 ± 0.04 to 7.04 ± 0.09 and intracellular pH in breast epithelial organoids by ~0.15.
TumCG↝, Breast tumors develop with median latency of 85.5 ± 8.2 days in NaHCO3-treated mice vs. 82 ± 7.5 days in control mice.
TumCP↑, accelerates proliferation without net effect on breast cancer development or tumor growth.

5613-

NaHCO3,

The Potential Role of Systemic Buffers in Reducing Intratumoral Extracellular pH and Acid-Mediated Invasion

Study,

Var,

pH↑, consequent reduction of tumor acid concentrations significantly reduces tumor growth and invasion without altering the pH of blood or normal tissues.
TumCG↓,
TumCI↓,
selectivity↑,

5612-

NaHCO3,

immuno,

Neutralization of tumor acidity improves anti-tumor responses to immunotherapies

vitro+vivo,

Var,

B16-F10

mice

Imm↑, Notably, neutralizing tumor acidity with bicarbonate monotherapy impaired the growth of some cancer types in mice where it was associated with increased T cell infiltration.
eff↑, Further, combining bicarbonate therapy with anti-CTLA-4, anti-PD1 or adoptive T cell transfer improved antitumor responses in multiple models, including cures in some subjects.
e-pH↑, In vivo, the acidic extracellular pH of tumors can be increased by providing mice with 200 mM ad lib sodium bicarbonate (bicarb) in drinking water
TumCG↓, However, in a transgenic (TRAMP) model of prostate cancer, bicarb therapy was shown to impair tumor development and subsequent metastases (41)
TumMeta↓,
eff↑, Notably, bicarb in combination with either checkpoint inhibitor was as effective in suppressing tumor growth as the two-checkpoint inhibitor combination

5599-

NaHCO3,

Acidity generated by the tumor microenvironment drives local invasion

in-vivo,

BC,

MDA-MB-231

Eight-to ten-week old severe combined immunodeficient (SCID) mice

in-vitro,

CRC,

HCT116

e-pH↑, oral administration of sodium bicarbonate was sufficient to increase peritumoral pH and inhibit tumor growth and local invasion in a preclinical model, supporting the acid-mediated invasion hypothesis.
TumCG↓, This pattern was observed across all five tumors in this study, wherein growth was highly correlated (p<0.02) with acidic pH below a threshold that varied from pH 6.8–7.1 in individual mice
TumCI↓, Acidic pHe can induce release of (cysteine or aspartyl) cathepsin proteinase activity in vitro (7–9), which is generally believed to be involved in local invasion and tissue remodeling
Dose↝, control group drank tap water and the experimental group was provided with 200 (mM) of NaHCO3 ad libitum.

5610-

NaHCO3,

doxoR,

Sodium bicarbonate nanoparticles modulate the tumor pH and enhance the cellular uptake of doxorubicin

vitro+vivo,

BC,

4T1

mice bearing orthotropic 4T1 breast cancer tumors

pH↑, In this study, 100-nm liposomes loaded with sodium bicarbonate were used as adjuvants to elevate the tumor pH. Mice administered bicarbonate-loaded liposomes reached an intra-tumor pH value of 7.38±0.04.
Imm↑, analysis of the tumor microenvironment demonstrated an increase in immune cell’ population (T-cell, B-cell and macrophages) in tumors treated with liposomal bicarbonate.
eff↑, This study demonstrates that targeting metabolic adjuvants with nanoparticles to the tumor microenvironment can enhance anticancer drug activity and improve treatment.
ChemoSen↑, Bicarbonate enhances the uptake and activity of doxorubicin by breast cancer cells
TumVol↓, Comparing the tumor sizes of all the experimental time-points (1-21 days post treatment) confirmed that mice treated with a sub-therapeutic doxorubicin dose plus bicarbonate had the slowest disease progression
eff↑, nanoparticle-targeted delivery of sodium bicarbonate can increase bicarbonate accumulation in the tumor tissue while decreasing the risks of adverse effects and toxicity.

5609-

NaHCO3,

Alkalization of cellular pH leads to cancer cell death by disrupting autophagy and mitochondrial function

in-vitro,

Var,

eff↑, We then reported that alternate infusion of bicarbonate and anticancer agent into tumors via tumor feeding artery markedly enhanced the efficacy of transarterial chemoembolization (TACE) in the local control of hepatocellular carcinoma (HCC).
e-pH↑, Alkalizing cellular pH by bicarbonate decreased pH gradient (ΔpH), membrane potential (ΔΨm), and proton motive force (Δp) across the inner membrane of mitochondria;
MMP↓,
OXPHOS↝, disruption of oxidative phosphorylation (OXPHOS) due to collapsed Δp
AMP↑, led to a significant increase in adenosine monophosphate (AMP), which activated the classical AMPK-mediated autophagy.
TumAuto↑,
MPT↑, Bicarbonate also induced persistent mitochondrial permeability (MPT) and damaged mitochondria.
mtDam↑,

5608-

NaHCO3,

Sodium Bicarbonate Nanoparticles for Amplified Cancer Immunotherapy by Inducing Pyroptosis and Regulating Lactic Acid Metabolism

Study,

Var,

TumCG↓, Collectively, NaHCO3 NPs observably inhibit primary/distal tumor growth and tumor metastasis through acid neutralization remitted immunosuppression and pyroptosis induced immune activation
TumMeta↓,
e-pH↑,
Pyro↑,
Imm↑,
Na+↑, t can further release high amounts of Na+ ions inside tumor cells

5607-

NaHCO3,

Does Baking Soda Function as a Magic Bullet for Patients With Cancer? A Mini Review

Review,

Var,

AntiCan↑, Sodium Bicarbonate “Kills” Cancer Cells
e-pH↑, The utilization of sodium bicarbonate to neutralize the acidity and increase the tumor pHe might control cancer cells progression
TumMeta↓, Sodium bicarbonate reduces the formation of spontaneous metastases and the rate of lymph node involvement in mouse models of metastatic breast cancer.
TumCI↓, administration of 200 mM bicarbonate to 4-week-old TRAMP mice (weaning at 3 weeks) effectively perturbs the in situ evolution of cancer to a microinvasive disease
TumCG↓, sodium bicarbonate significantly controls tumor growth and improves CD8+ T-cell infiltration.
CD8+↑,
NK cell↑, Natural killer (NK) cell activity is also increased in a B-cell lymphoma mouse model following the systemic administration of a buffer therapy.
Remission↑, began a self-administered course of vitamins, supplements, and 60 g of bicarbonate mixed in water daily. As of this submission, he has remained well with stable tumor for 10 months.
eff↑, Therefore, sodium bicarbonate could be used as an adjuvant therapy to enhance the efficacy of conventional treatments.
ChemoSen↑, Surprisingly, extracellular alkalization induced a 2- to 3-fold increase in the efficacy of doxorubicin
ChemoSen↓, it greatly reduces the efficacy of some weak acidic chemotherapeutics, such as chlorambucil.

5604-

NaHCO3,

Mitochondrial metabolic reprogramming of macrophages and T cells enhances CD47 antibody-engineered oncolytic virus antitumor immunity

vitro+vivo,

Melanoma,

B16-BL6

Six-week-old female BALB/c mice and C57BL/6 J mice

in-vitro,

BC,

4T1

eff↑, identified sodium bicarbonate (NaBi) as the potent metabolic reprogramming agent that enhanced antitumor responses in the acidic TME.
eff↑, NaBi and oAd-αCD47 therapy significantly inhibited tumor growth and produced complete immune control in various tumor-bearing mouse models.
TumMeta↓, suggesting its potential as an effective neoadjuvant treatment for preventing postoperative tumor recurrence and metastasis.
pH↑, NaBi improves the acidity of the TME and activates the CaMKII/CREB/PGC1α mitochondrial biosynthesis signaling pathway
CaMKII ↑,
CREB↑,
PGC-1α↑, NaBi increases the mitochondrial content of T cells and BMDMs by promoting the expression of PGC1α mediated by the Ca2+-CaMKII-CREB signaling pathway in an LA environment
AntiTum↑, oral NaBi enhances the antitumor effect of oAd-αCD47.
Imm↑, We proposed that sodium bicarbonate (NaBi) can act as an immunomodulator to reprogram metabolic disorders of CD8+ T cells and TAMs in an acidic environment.
CD8+↑, Combination therapy remodels the immunosuppressive microenvironment to promote activation of CD8+ T cells and TAMs
TAMS↑,

5603-

NaHCO3,

immuno,

Acidosis-mediated increase in IFN-γ-induced PD-L1 expression on cancer cells as an immune escape mechanism in solid tumors

in-vitro,

BC,

MCF-7

in-vitro,

PC,

MIA PaCa-2

in-vitro,

GBM,

U87MG

eff↑, These findings have important implications for the development of new strategies to enhance the efficacy of immunotherapy in cancer patients.
e-pH↑, In vivo studies fully validated our in vitro findings and revealed that neutralizing the acidic extracellular tumor pH by sodium bicarbonate treatment suppresses IFN-γ-induced PD-L1 expression and promotes immune cell infiltration in responsive tumor
PD-L1↓,

5602-

NaHCO3,

immuno,

Immunotherapy Enhancement by Targeting Extracellular Tumor pH in Triple-Negative Breast Cancer Mouse Model

in-vivo,

BC,

4T1

mouse

eff↑, n this study, oral administration of either sodium bicarbonate or sodium bicarbonate plus anti-PD-L1 combination enhanced responses to anti-tumor immunity by tumor growth inhibition and improving survival time in TNBC.
TumCG↓,
OS↑,
e-pH↑, Here, we show that NaHCO3 increased extracellular pH (pHe) in tumor tissues in vivo
IFN-γ↑, an effect that was accompanied by an increase in T cell infiltration, T cell activation and IFN-γ, IL2 and IL12p40 mRNA expression in tumor tissues
IL2↑, The expression of IFN-γ, IL-2 and IL-12 mRNA was significantly increased in response to NaHCO3 alone
IL12↑,
Dose↝, The mice in group number three were given drinking water with 200 mM NaHCO3 to increase the pHe > 7.2 via bicarbonate-induced metabolic alkalosis
PD-L1↓, Sodium Bicarbonate Therapy Decreases Tumor PD-L1 Expression In Vivo

5601-

NaHCO3,

Tumor acidity, ion trapping and chemotherapeutics. II. pH-dependent partition coefficients predict importance of ion trapping on pharmacokinetics of weakly basic chemotherapeutic agents

vitro+vivo,

Var,

e-pH↑, We have previously demonstrated that chronic and acute treatment of tumor-bearing mice with sodium bicarbonate results in tumor-specific alkalinization of extracellular pH.
ChemoSen↑, Furthermore, bicarbonate pretreatment enhances the anti-tumor activity of doxorubicin and mitoxantrone in two different mouse tumor models.

5600-

NaHCO3,

Acidosis and Cancer: from Mechanism to Neutralization

Review,

Var,

e-pH↑, During this work we observed in multiple systems that chronic ingestion of ad lib 200 mM sodium bicarbonate increases tumor pH and rarely affects growth of primary tumors, but potently inhibited experimental or spontaneous metastases (61).
TumCG↝,
eff↑, In mice bearing B-16 melanoma xenografts, treatment with bicarbonate synergized with the T-cell checkpoint inhibitors anti-CTLA4 antibody (ipilimumab) and anti PD-1.

1671-

PBG,

Importance of pH Homeostasis in Metabolic Health and Diseases: Crucial Role of Membrane Proton Transport

Review,

Nor,

pH↑, obtained evidence that intake of propolis elevates the pH of ascites and metabolic tissues compared with normal diet,

1658-

PBG,

Body Fluid pH Balance in Metabolic Health and Possible Benefits of Dietary Alkaline Foods

Review,

Var,

pH↑, pH of ascites and interstitial fluids around metabolic tissues is improved (elevated) by the intake of propolis compared with normal diet
GFR↑, improved the estimated glomerular filtration rate

1659-

PBG,

Improvement of insulin resistance, blood pressure and interstitial pH in early developmental stage of insulin resistance in OLETF rats by intake of propolis extracts

in-vivo,

Nor,

rats

pH↑, found that interstitial fluid pH in ascites, liver, and skeletal muscle was higher in rats fed propolis diet than rats fed normal diet.
BP↓, Propolis significantly reduced systolic arterial pressures in both 0.1% and 0.5%-propolis contained diet groups compared with normal diet (p < 0.05)
BG↓, decreased levels of blood glucose and plasma insulin

Showing Research Papers: 1 to 27 of 27

* indicates research on normal cells as opposed to diseased cells
Total Research Paper Matches: 27

Pathway results for Effect on Cancer / Diseased Cells:

Infection & Microbiome ⓘ

CD8+↑, 2,
Total Targets: 76

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

antiOx↑, 1, GPx1↑, 1, GPx4↑, 1, OXPHOS↓, 1, ROS↓, 1, SOD1↑, 1,

Mitochondria & Bioenergetics ⓘ

mitResp↓, 1,

Core Metabolism/Glycolysis ⓘ

Glycolysis↑, 1, HK2↑, 1, PFKL↑, 1, PFKM↑, 1, PKM2↑, 1,

Transcription & Epigenetics ⓘ

other↝, 1, tumCV↑, 1,

Migration ⓘ

Ca+2↓, 1, TumCMig↑, 1,

Barriers & Transport ⓘ

GLUT1↑, 1,

Cellular Microenvironment ⓘ

pH↑, 1,
Total Targets: 18

Scientific Paper Hit Count for: pH,

19 Bicarbonate(Sodium)
4 immunotherapy
3 Propolis -bee glue
2 Curcumin
2 Magnetic Fields
1 Citric Acid
1 Dichloroacetate
1 doxorubicin

Query results interpretion may depend on "conditions" listed in the research papers.
Such Conditions may include : 
  -low or high Dose
  -format for product, such as nano of lipid formations
  -different cell line effects
  -synergies with other products 
  -if effect was for normal or cancerous cells

Filter Conditions: Pro/AntiFlg:%  IllCat:%  CanType:%  Cells:%  prod#:%  Target#:250  State#:%  Dir#:2
  wNotes=on  sortOrder:rid,rpid

pH Cancer Research Results

Pathway results for Effect on Cancer / Diseased Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Cell Death ⓘ

Kinase & Signal Transduction ⓘ

Transcription & Epigenetics ⓘ

Autophagy & Lysosomes ⓘ

DNA Damage & Repair ⓘ

Proliferation, Differentiation & Cell State ⓘ

Migration ⓘ

Angiogenesis & Vasculature ⓘ

Barriers & Transport ⓘ

Immune & Inflammatory Signaling ⓘ

Cellular Microenvironment ⓘ

Drug Metabolism & Resistance ⓘ

Clinical Biomarkers ⓘ

Functional Outcomes ⓘ

Infection & Microbiome ⓘ

Pathway results for Effect on Normal Cells:

Redox & Oxidative Stress ⓘ

Mitochondria & Bioenergetics ⓘ

Core Metabolism/Glycolysis ⓘ

Transcription & Epigenetics ⓘ

Migration ⓘ

Barriers & Transport ⓘ

Cellular Microenvironment ⓘ

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